Key result
Exendin-4 reduces myocardial injury markers and improves mitochondrial function in diabetic mice.
Why the study?
Does exendin-4 improve diabetic cardiomyopathy in a mouse model?
RCT
Randomly divided
Does exendin-4 improve diabetic cardiomyopathy in a mouse model?
Exendin-4 protects against myocardial injury in diabetic mice by improving mitochondrial function and inhibiting oxidative stress through the Sirt1/PGC1α signaling pathway.
Answers are grounded in this paper and cite their sources.
Exendin-4 signals merit further mechanistic study in diabetic cardiomyopathy; leaves open any human translation or practice change.
OBJECTIVE: To investigate the protective effect of exendin-4 against diabetic cardiomyopathy in mice and explore the underlying mechanism. METHODS: C57BL/6J mice were randomly divided into normal control group with normal diet and diabetic group with high-fat diet for 4 weeks before streptozotocin injection. The successfully established diabetic mouse models were divided into diabetic group with exendin-4 treatment and diabetic control group for daily treatment with intraperitoneal injection of 1 nmol/kg exendin-4 and saline of equivalent volume for 8 weeks, respectively. The physiological parameters such as blood glucose and body weight were recorded. RT-PCR was used to examine the transcription levels of genes related with myocardial hypertrophy and fibrosis and the genes related with mitochondrial functions including PGC1α, NRF and CytoC. The expressions of oxidative stress markers and Sirt1/PGC1 proteins were measured using Western blotting. and HE staining was used to observe the myocardial structural changes in the mice. RESULTS: Compared with the normal control mice, the mice in diabetic control group showed significantly increased blood glucose and blood lipid levels (P<0.001), which were obviously improved by Exendin-4 treatment. The expressions of ANP, BNP, TGFβ1, CytoC1 and NOX1 were significantly increased (P<0.05) while Sirt1, PGC1α, NRF and SOD1 expression were markedly decreased in the myocardial tissue of the diabetic mice (P<0.05). Exendin-4 treatment resulted in obviously reduced expressions of ANP, BNP, TGFβ1, CytoC1 and NOX1 (P<0.05) and increased expressions of Sirt1, PGC1α, NRF and SOD1 (P<0.05) in the diabetic mice. CONCLUSIONS: Exendin-4 protects against myocardial injury in diabetic mice by improving mitochondrial function and inhibiting oxidative stress through the Sirt1/PGC1α signaling pathway.
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Cai et al. (2018) conducted an RCT in Diabetic cardiomyopathy. Exendin-4 vs. Saline was evaluated on Myocardial hypertrophy, fibrosis, and mitochondrial function markers (p=<0.05). Exendin-4 treatment reduced expressions of myocardial injury markers (ANP, BNP, TGFβ1) and increased mitochondrial function markers (Sirt1, PGC1α) in diabetic mice.
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